Review
Parasitic infections of the lung: a guide for the
1
Department of Respiratory
Medicine, Birmingham
Heartlands Hospital,
Birmingham, UK
2
Department of Clinical
Parasitology, Hospital for
Tropical Diseases, London, UK
3
Department of Respiratory
Medicine, St Mary’s Hospital,
Imperial College Healthcare NHS
Trust, London, UK
4
Department of Radiology,
Birmingham Heartlands
Hospital, Birmingham, UK
5
Department of Clinical
Research, London School of
Hygiene and Tropical Medicine
and Hospital for Tropical
Diseases, London, UK
Correspondence to
Heinke Kunst, Department of
Respiratory Medicine,
Birmingham Heartlands
Hospital, Bordesley Green East,
Birmingham B9 5SS, UK;
hkunst@doctors.org.uk
Received 29 November 2009
Accepted 28 May 2010
Published Online First
29 September 2010
528
respiratory physician
H Kunst,1 D Mack,2 O M Kon,3 A K Banerjee,4 P Chiodini,2,5 A Grant5
ABSTRACT
Parasitic infections of the lung occur worldwide among
both immunocompetent and immunocompromised
patients and may affect the respiratory system in
a variety of ways. This review provides an update on the
presenting symptoms, signs, investigation and
management of diseases affecting the lung caused by
protozoa, nematodes and trematodes. The clinical
presentations and radiographic findings of several of
these diseases may mimic tuberculosis and malignancy.
It is important to consider parasitic infections in the
differential diagnosis of such lung diseases. If identified
early, most parasitic diseases that affect the lung are
curable with medical or surgical treatments.
INTRODUCTION
With increasing travel and migration, rates of
parasitic lung and pleural diseases are increasing in
the immunocompetent population in developed
countries as well as among immunocompromised
patients. Respiratory physicians should consider
parasitic diseases in the differential diagnosis of
lung conditions such as tuberculosis and malig-
nancy, with which parasitic lung diseases may be
confused.
This review describes the presentation, investi-
gation and management of common parasitic
infections affecting the lung caused by protozoa,
nematodes and trematodes. The diseases have been
grouped according to their manner of presentation:
(1) those presenting with focal lesions and (2) those
which characteristically present with diffuse lung
disease. Focal lung lesions have been divided into
cystic lung lesions, coin lesions and consolidation/
pleural effusion. Diffuse lung disease has been
divided into transient pulmonary infiltrates and
alveolar/interstitial lung changes. Diseases that
may present in a variety of ways are fully described
only the first time they are mentioned.
CONDITIONS PRESENTING WITH FOCAL LUNG
LESIONS
Cystic lung lesions
Hydatidosis
Distribution and life cycle
Hydatid disease is caused by larvae of Echinococcus
tapeworm species, the definite hosts of which are
members of the Canidae family (dogs and foxes).
Most cases are caused by Echinococcus granulosus
which has a worldwide distribution including
South America, countries surrounding the Medi-
terranean, the Middle East, some sub-Saharan
African countries, Russia and China. Although
most cysts form in the liver, 20e30% form in the
lung.
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Dogs are the definitive host for E granulosus and
harbour the adult worms in their gut. The eggs
shed in dog faeces remain viable for many weeks
and are able to contaminate food sources of inter-
mediate hosts such as sheep, cattle and horses.
When humans become accidental intermediate
hosts after eating food contaminated with eggs, the
ingested eggs hatch, releasing larvae which migrate
from the gastrointestinal tract to the circulation.
The eggs travel to the liver or lungs and slowly
develop into hydatid cysts over a period of several
months or years. Occasionally, lung cysts form
after transdiaphragmatic spread of parasites
following the rupture of liver cysts.
Presentation
Primary infection is asymptomatic and patients
may remain asymptomatic for years, during which
time lung lesions may be discovered incidentally on
a chest x-ray. In Europe the average patient is in
their 30s at diagnosis.1 Cysts may cause symptoms
by compression of adjacent structures, and lung
cysts may present with chest pain, cough,
haemoptysis or pneumothorax. Symptoms may
also occur if antigenic material is released from the
cyst, causing a hypersensitivity reaction with fever,
wheeze and urticaria and, rarely, anaphylaxis. Cysts
may become secondarily infected causing empyema
or lung abscess formation.
Imaging features
Cysts can be seen as single or multiple well-defined
homogenous lesions surrounded by otherwise
normal lung parenchyma on a plain chest x-ray.
The lower lobes, posterior lung segments and the
right lung are affected most frequently.2 The cyst
wall often calcifies over time. A CT scan of the
chest may reveal further diagnostic features
including collapse of the laminated membrane from
the surrounding host tissue, the presence of
daughter cysts and the presence of cyst rupture.3
Air between the host tissue and laminated
membrane of ruptured cysts may produce crescent-
shaped lucencies. A pleural effusion or a hydro-
pneumothorax may develop following the rupture
of a pulmonary cyst into the pleural space.
Collapsed laminated membrane may float in the
cyst cavity, producing the ‘water lily’ sign (figures 1
and 2).3 4
Laboratory diagnosis
Peripheral blood eosinophilia may be found in no
more than 50% of cases. A substantial rise in
eosinophil count is often associated with a leakage
of antigenic material from the cyst. Serological tests
to support the initial diagnosis are available at
reference laboratories but are less sensitive for the
diagnosis of lung disease than for hepatic disease.1
Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217

Figure 1 Chest x-ray showing a hydatid cyst in the left lower lobe with
a collapsed hydatid cyst exhibiting the ‘lily pad’ sign lying above it.
Postoperatively, serological tests may be used to monitor the
immunological response to treatment.5
While percutaneous aspiration of liver cysts under ultrasound
guidance can support the diagnosis by demonstrating the pres-
ence of protoscolices or hooklets, this is not generally recom-
mended because of the risk of leakage resulting in an
anaphylactic reaction.
Management
6 There are no reliable serological tests available commercially.
In a small number of cases hydatid cysts resolve spontaneously.
In the majority of cases the treatment of choice is surgical
excision of cysts with a view to preserve as much lung paren-
chyma as possible.7 Albendazole should be avoided preopera-
tively as it may soften the cyst wall and increase the chance of
rupture. It may be given as adjunctive therapy once the cyst has
been removed.8 When surgery is contraindicated or not feasible
in patients with multiorgan involvement, medical treatment
with albendazole with or without praziquantel is recom-
mended.9 Expert advice should be sought regarding chemother-
apeutic regimens before and after surgery and for cases where
surgery is not to be carried out. While aspiration followed by
injection of a scolicidal agent and re-aspiration (PAIR) has been
used as a therapeutic tool when surgery is contraindicated,10 the
World Health Organization states that PAIR is contraindicated
for lung cysts11 and the authors endorse that view.
Figure 2 CT scan of the thorax showing a ruptured hydatid cyst in the
left upper lobe of the lung.
Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217
Review
Coin lesions
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Dirofilariasis
Distribution and life cycle
Pulmonary dirofilariasis is caused by the dog heartworm Diro-
filaria immitis and has been reported from Japan, Australia, the
USA and Italy (D repens). Adult worms live in the right ventricle
of the definitive canine hosts and produce circulating microfilaria
which can be transmitted by a variety of mosquito species to
humans. In humans the worms pass through the right ventricle
but fail to mature and are swept away to peripheral pulmonary
arteries.
Presentation
Most patients are asymptomatic, although symptoms including
chest pain, cough, haemoptysis, wheezing, fever, chills and
malaise have been reported.12
Imaging features
The most common presentation is with a coin lesion on chest
radiography. These are usually 1e3 cm in diameter and sharply
defined. In established lesions a central necrotic area is
surrounded by a granulomatous reaction and fibrous wall.13
Dead worms may calcify. Positron emission tomographic scan-
ning may show an increased uptake of fluorodeoxyglucose
around necrotic nodules, a feature also seen in other infectious
lung nodules.14
Laboratory diagnosis
Eosinophilia may be present in a small number of patients.
Most cases are diagnosed by identifying the worm in biopsy
specimens after thoracatomy for a pulmonary nodule thought to
be a malignancy.15
Management
Chemotherapy is ineffective. The only treatment is surgical
excision if indicated.
Consolidation/pleural effusion
Paragonimiasis
Distribution and life cycle
Pulmonary paragonimiasis is most frequently seen in south east
Asia but also occurs in central Africa and South America. It is
caused by lung flukes of the genus Paragonimus. Paragonimus
westermani is responsible for most cases. The adult worms are
found in pulmonary cysts, usually in pairs. Adult worms
produce eggs which are secreted in sputum or faeces. Humans
are usually infected by eating the second intermediate host,
fresh water crab or crayfish, if raw or lightly cooked. After
ingestion the larvae penetrate the intestinal wall and migrate to
the lung parenchyma. They mature in a fibrous host-derived
capsule, usually in the upper zones of the lung.
Presentation
Presenting symptoms include pleuritic chest pain, haemoptysis,
chronic cough and fever. If pulmonary cysts erode into adjacent
bronchi, patients may suffer life-threatening haemoptysis.16
Imaging features
Radiographic features of paragonimiasis include patchy air space
consolidation, cystic changes and ring shadows. Pleural effusions
and pneumothoraces may occur. On the CT scan round low-
attenuation cystic lesions filled with fluid or gas may be seen
within an area of consolidation. Peripheral linear opacities seen
on chest x-rays are suggestive of worm migration tracks on
corresponding CT scans. Intracystic worms may be detected on
a CT scan of the thorax.17 18 Patients with pulmonary
529
 Review

paragonimiasis who present with parenchymal lesions on a CT formation which carries a mortality of 15e35%.25 Infiltration of

Thorax: first published as 10.1136/thx.2009.132217 on 29 September 2010. Downloaded from http://thorax.bmj.com/ on May 9, 2021 by guest. Protected by copyright.
scan of the thorax may have bronchial stenosis on broncho- the lung parenchyma may result in pneumonia or lung abscess
scopy.19 Paragonimiasis is often misdiagnosed as tuberculosis or formation. Furthermore, a hepatobronchial fistula leading to
malignant disease and should be considered in the differential expectoration of ‘anchovy sauce-like’ purulent sputum can
diagnosis of these conditions in those who have lived in endemic develop. Rarely, a bronchobiliary fistula may occur causing bile
countries.20e22 expectoration.
Laboratory diagnosis Radiographic features
Peripheral blood eosinophilia is mainly seen during larval Common radiological features include right pleural effusion and
migration through the lung and total serum IgE may be raised. basal lung disease. Right lower lobe consolidation may develop,
The eosinophil counts are usually elevated in pleural and bron- which may progress to abscess formation (figure 3).
choalveolar lavage fluids. The identification of the characteristic
Laboratory investigations
operculated eggs in faeces, sputum or bronchoalveolar lavage
Eosinophilia is not a feature of amoebic infections. If symptoms
fluid confirms the diagnosis. Specific serological testing is not
of dysentery are present, freshly passed stools should be exam-
performed in the UK but samples may be referred to overseas
ined for amoebic trophozoites. Trophozoites are seldom found in
laboratories for specific IgG and IgM antibody testing when
sputum, pleural fluid or abscess aspirates. Antibodies directed
paragonimiasis is suspected.20 23
against the parasite may be detected by a variety of methods.
Management Antibody tests start to become positive after approximately
Medical treatment is usually with praziquantel. Some patients 1 week and have a sensitivity of 95% for the diagnosis of
may require surgery for persistent pneumothorax, pleural effusion amoebic liver abscess but are only positive in approximately 75%
or empyema.24 of cases of intestinal infection. The E histolytica adhesin may be
detected in faecal specimens by ELISA. This test is also helpful in
Amoebiasis differentiating between E histolytica and E dispar in asymptom-
Distribution and life cycle atic patients who pass amoebic cysts.
Amoebiasis is caused by Entamoeba histolytica, a protozoan found
Management
worldwide. E histolytica is the causative agent of invasive
Medical treatment consists of a course of tinidazole or metro-
amoebiasis but is morphologically indistinguishable from
nidazole to kill trophozoites in tissue, followed by diloxanide
a related but non-pathogenic species, E dispar. E histolytica is
furoate or paromomycin to eliminate cysts from the intestinal
endemic in regions with poor sanitation and poor socioeconomic
lumen.28 29 Surgical treatment of pulmonary amoebiasis may be
conditions. The motile trophozoite forms of the parasite live in
required when there is direct pulmonary involvement or spread
the lumen of the large intestine where they multiply and
to pleura.
differentiate into the cyst forms. Cysts are passed in the faeces
and are highly resistant to environmental conditions, facilitating
faecal-oral transmission. Ingested cysts are transformed into CONDITIONS PRESENTING WITH DIFFUSE LUNG DISEASE
trophozoites. Transient pulmonary infiltrates
Ascariasis
Presentation Distribution and life cycle
In most infections the organism does not invade the gut mucosa. Ascariasis is caused by Ascaris lumbricoides, the round worm. It is
In a subset of cases the E histolytica trophozoites bind to intes- common worldwide in areas with poor sanitation where there is
tinal epithelial cells via a lectin expressed on the parasite surface. faecal contamination of soil or food. Transmission of the disease
This leads to lysis of the epithelial cells and invasive amoebiasis is faecal-oral. After eggs are ingested they hatch and larvae
resulting in colitis. Blood-borne spread of the parasite may lead migrate via the portal circulation to the liver then via the heart
to the formation of an amoebic liver abscess which may present to reach the lungs 2 weeks after ingestion. Larvae then ascend to
several months after the initial infection when diarrhoea may be the trachea, are swallowed and eventually develop into adults in
absent. the small intestine, producing eggs 10e12 weeks after ingestion.
Amoebic liver abscess may cause irritation of the diaphragm
and the patient may present with cough. A serous pleural
effusion may occur in conjunction with an amoebic liver abscess
and does not indicate extension of the disease.25 Amoebic liver
abscess may also present with chest pain due to hepatic
enlargement and inflammation. Elevation of the hemidiaphragm
can cause segmental atelectasis of the lung and lead to secondary
bacterial pneumonia.26
Amoebic pleuropulmonary disease is the most common
complication of amoebic liver abscess, occurring in 15% of
patients with amoebic liver disease and in 1% of patients with
amoebic dysentery.27 It most commonly occurs by direct
extension from a superior right lobe hepatic abscess through the
diaphragm into the right lower lobe of the lung, presenting with
cough, pleuritic pain and dyspnoea.25 Pleuropulmonary amoe-
biasis may also occur following haematogenous spread of
organisms to the lungs or lymphatic spread from the liver to the
diaphragm. Intrathoracic complications include rupture of an Figure 3 Chest x-ray showing right basal consolidation and pleural
amoebic liver abscess into the pleural cavity with empyema effusion secondary to amoebic liver abscess.

530 Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217


Presentation
During the second week of infection, as the larvae invade the
lung tissue, a small proportion of patients become symptomatic.
Loeffler’s syndrome is caused by larval migration into the alveoli
which triggers an allergic response leading to respiratory
symptoms including cough, wheeze, dyspnoea, chest pain, fever
and haemoptysis. The illness usually resolves spontaneously
after several weeks.
Imaging features
During pulmonary migration, transient nodular or diffuse
pulmonary infiltrates on the chest x-ray support the diagnosis of
Loeffler’s syndrome. Chronic eosinophilic pneumonia has been
associated with ascariasis of the lung.30 Spontaneous pneumo-
thoraces have been described infrequently.31
Laboratory diagnosis
During larval migration a leucocytosis and peripheral blood
eosinophilia are often present and total serum IgE may be
elevated. Eosinophils and larvae may be found in sputum. The
diagnosis is confirmed by finding characteristic Ascaris eggs in
the stool on microscopy, although these may not be passed until
after resolution of the pulmonary symptoms. Serological tests
are not routinely available.
Management
A single dose of albendazole is the treatment of choice. Meben-
dazole, piperazine and pyrantel pamoate are alternatives.28
Hookworm infections
Distribution and life cycle
Ancylostomiasis is common in tropical and subtropical coun-
tries, caused by two species of hookworm (Ancylostoma duodenale
and Necator americanus). A duodenale is also found in the Middle
East and southern Europe; N americanus is found sporadically in
the southeastern USA. Hookworm eggs are passed in faeces and
develop in soil into filariform larvae able to penetrate the skin of
the human host. Poor sanitation and the absence of footwear
favour transmission. The larvae penetrate blood vessels and
undergo heartelung migration before breaking out into the
alveoli and ascending to the pharynx from where they are
swallowed. The hookworms subsequently mature into adults in
the small intestine. Eggs first appear in the stool 5 weeks after
skin invasion.
Presentation
Pulmonary manifestations are usually mild. During larval
migration in the lung the hookworm may cause symptoms and
signs consistent with Loeffler’s syndrome including dry cough,
wheeze, dyspnoea and fever.
Imaging features
The radiographic changes are consistent with Loeffler’s
syndrome and an eosinophilic pneumonia with transient
non-segmental areas of consolidation.13
Laboratory diagnosis
Peripheral blood eosinophilia is found during larval migration
and commonly persists during gastrointestinal infection.
Although their appearance may be delayed, finding eggs in the
stool supports the diagnosis. Serological tests are not useful in
view of many cross-reactions with other helminthic infections.27
Management
Recommended treatment consists of a single dose of albenda-
zole. Mebendazole and pyrantel pamoate are alternatives.28
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Review
Toxocariasis
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Distribution and life cycle
Human toxocariasis is usually caused by the dog round worm
Toxocara canis which commonly infects juvenile dogs and has
a worldwide distribution. Humans, who are incidental hosts, are
usually infected by the ingestion of eggs. The disease primarily
affects children, who acquire the infection through contact with
soil contaminated with embryonated eggs. Fresh animal faeces
are not infectious as the eggs require 2e3 weeks to embryonate
in the soil. Ingested eggs hatch in the stomach. Larvae penetrate
the mucosa of the gut and enter the mesenteric vessels from
where they migrate to the lungs and other organs.
Presentation
Most infections occur in children and most are asymptomatic.
Patients may present with immunologically-mediated symp-
toms including cough, dyspnoea and wheeze which may present
as asthma or bronchitis. Presenting signs may include hepato-
megaly, splenomegaly and ocular lesions.
Radiographic features
Radiological features may include transient localised changes or
widespread patchy areas of consolidation.13
Laboratory diagnosis
Toxocara larvae do not develop into adults in the human host, so
eggs are not passed in human faeces. Visceral larva migrans is
characterised by persistent peripheral eosinophilia and leuco-
cytosis. A high degree of eosinophilia in the differential cell
count of bronchoalveolar lavage fluid may support the diag-
nosis.32 33 Serological tests are available at reference laboratories.
Although positive Toxocara serology supports a diagnosis of
visceral larva migrans, titres may remain elevated for years and
other causes of illness should be considered.34 Children
suspected of ingesting infective Toxocara eggs may be investi-
gated with full blood count and Toxocara serology tests at
baseline and at 3 months. In practice this is seldom required as,
in many cases where dog faeces have been ingested, it is possible
to establish that the sample is relatively fresh and thus not likely
to contain embryonated eggs. Tissue biopsy is not required for
the diagnosis of visceral larva migrans.
Management
Ocular disease is treated under the supervision of an ophthal-
mologist with local or systemic steroids. Anthelminthics are not
usually given. Visceral larva migrans is treated with albendazole.
Corticosteroids may be required in more severe cases.28
Alveolar/interstitial changes
Schistosomiasis
Distribution and life cycle
Schistosomiasis is endemic throughout the tropics and it is
estimated that more than 200 million people worldwide are
infected.35 There are three main species of schistosomes: Schis-
tosoma mansoni, Schistosoma haematobium and Schistosoma japo-
nicum. The adult trematode worms are found in the vesical
plexus (S haematobium) or in the mesenteric veins (S mansoni and
S japonicum). Their eggs are excreted in urine or faeces respec-
tively. Humans are infected by cercariae during contact with
fresh water. The organisms enter the circulation and pass
through the heart, lungs and then the liver to reach the target
venous plexus. There the worms mature and mate, releasing
eggs 4e6 weeks after skin penetration. The initial release of eggs
may give rise to acute schistosomiasis which occurs predomi-
nantly in non-immune hosts. Eggs that are not passed into the
531
 Review
bladder or intestinal lumen are the main cause of chronic disease,
causing granulomatous reactions and fibrosis. In severe long-
standing S mansoni and S japonicum infections, the development
of hepatosplenomegaly and portal hypertension may lead to
diversion of eggs to the lung vasculature. This results in oblit-
erative arteritis which may cause pulmonary hypertension.
Presentation
In non-endemic countries, returned non-immune travellers may
present with acute schistosomiasis while migrants from endemic
countries may present with chronic disease. Acute schistosomiasis
(Katayama fever) may present with fever, cough, dyspnoea, rash
and arthralgias.36 The precise pathogenesis of Katayama fever is
unknown, but it is thought to be due to an immune complex
phenomenon initiated by eggs laid by maturing schistosomes.
Typically, symptoms occur 4e6 weeks after infection. In acute
schistosomiasis, serological tests are often negative and eggs are not
detectable, requiring the diagnosis to be made on clinical and
epidemiological grounds. In heavy infections, the migratory phase
through the lungs may produce a pneumonitis resembling that
produced during hookworm migration. A Loeffler-like syndrome
may occur during the treatment of heavy infections. Acute symp-
toms are usually self-limiting. In the chronic stage the commonest
symptoms are dyspnoea, reduced exercise tolerance and chest pain.
Clinical signs of severe hypoxaemia such as digital clubbing may be
seen. Since schistosomiasis is an important cause of pulmonary
hypertension, it should always be considered as a differential
diagnosis in patients from endemic countries.37 The chronic form of
schistosomiasis may also cause pulmonary arteriovenous fistulas.38
Radiological features
Nodular ill-defined lesions or reticulonodular changes may be
seen on the chest x-ray in acute pulmonary schistosomiasis
(figure 4).39 Although radiological findings are usually transitory
in acute infection, chest x-rays may show features resembling
granulomatous disease or tuberculosis.40 41 In chronic lung
disease, interstitial or granulomatous changes are caused by the
widespread deposition of eggs in the pulmonary vasculature. A
CT scan of the thorax may show nodular changes and ground
glass opacification (figure 5).42
Figure 4 Chest x-ray showing widespread pulmonary nodules in
pulmonary schistosomiasis. Reproduced with permission from Waldman
et al.42
532
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Figure 5 CT scan of the thorax showing the halo sign in pulmonary
schistosomiasis.
Laboratory investigation
Peripheral blood eosinophilia is present in more than 65% of
patients.43 Eggs of the Schistosoma species may be found in
faeces, urine and sputum or bronchoalveolar lavage 6 weeks after
infection. Eggs of S haematobium are most likely to be found in
late morning urine samples.44 Terminal urine specimens maxi-
mise sensitivity.45 IgG antibodies to Schistosoma egg antigen are
detectable 6e12 weeks following infection and can be measured
by ELISA. Such assays have sensitivities of >90% for the diag-
nosis of schistosomiasis.46 These tests may remain positive for
several years and are not helpful for monitoring response to
treatment. Serological testing in asymptomatic travellers should
be delayed for a period of 3 months following exposure to fresh
water to allow time for seroconversion. Schistosomal serology
may be negative, especially in Katayama fever, but if positive it
provides helpful diagnostic information.43 47
Management
The treatment of choice for schistosomiasis is praziquantel.28 48
In acute schistosomiasis (Katayama fever) praziquantel is
administered under steroid cover. A second course of prazi-
quantel may need to be given 3e6 months later to eradicate any
schistosomes that may have survived the first course of treat-
ment.47 Treatment is less beneficial in advanced chronic disease.
Strongyloidiasis
Distribution and life cycle
Strongyloidiasis is caused by the nematode Strongyloides stercor-
alis and is prevalent in tropical and subtropical countries.
Filariform larvae penetrate the skin, enter blood vessels and
undergo heart and lung migration. They migrate into alveoli
and subsequently ascend to the trachea. Larvae are swallowed
and develop in the small intestine into adult worms which
produce eggs. These are deposited in the intestinal mucosa
where they hatch into rhabditiform larvae which are excreted in
faeces. Occasionally, rhabditiform larvae mature to the filariform
stage while still in the bowel lumen. These filariform larvae may
penetrate the bowel wall or the perianal skin to initiate a new
cycle (autoinfection). Thus, in the absence of treatment, an
individual may harbour Strongyloides for several decades.
Presentation
Clinically the infection is often asymptomatic, but mild symp-
toms may occur in the initial stages of lung migration. In the
immunocompromised patient (including those on steroid
Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217
 Table 1 Overview of parasitic lung diseases
Condition Presentation
Focal disease
Cystic lesions
Hydatidosis Symptoms due to mass
effect
Chest pain, cough,
haemoptysis
Hypersensitivity reaction
Secondary abscess
formation
Coin lesions
Dirofilariasis Chest pain, cough,
haemoptysis, wheezing
Fever, malaise
Consolidation/pleural effusion
Paragonimiasis Pleuritic chest pain, cough,
Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217
fever, haemoptysis
Amoebiasis Right upper quadrant or
shoulder tip pain
Cough and bile expectoration
Diffuse disease
Transient pulmonary
infiltrates
Ascariasis Cough, wheeze, dyspnoea,
chest pain, fever
Loeffler’s syndrome
Haemoptysis
Hookworm infection Cough, wheeze, dyspnoea,
chest pain, fever
Loeffler’s syndrome
Toxocariasis Cough, dyspnoea, wheeze,
asthma or bronchitis
Hepatomegaly,
splenomegaly, ocular lesions
Alveolar/ interstitial changes
533
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Imaging features
Single or multiple lung cysts
Pleural effusion
Pneumothorax
Hydro-pneumothorax
Coin lesion with or without
calcification
Pulmonary infiltrates
Consolidation or cystic
lesions
Pleural effusion
Pneumothorax
Pleural effusion, atelectasis,
Empyema
Amoebic lung abscess
Secondary pneumonia
Hepatobronchial fistula
Transient pulmonary
infiltrates
Bacterial pneumonia,
eosinophilic pneumonia
Pneumothorax
Transient pulmonary
infiltrates
Eosinophilic pneumonia
Pulmonary infiltrates
Secondary bacterial
pneumonia
Geographical distribution
Wide distribution:
Mediterranean borders,
East and Central Asia,
sub-Saharan Africa, Russia,
China, South America
Pulmonary dirofilariasis
reported from USA, Japan,
Australia, South America
Asia, West Africa, Central
and South America
Widely distributed
Worldwide in areas where
sanitation is poor (faecal-oral
transmission)
Widely distributed: (infection
usually by contact of bare
feet with faecally
contaminated soil)
Worldwide distribution (adult
worms live in gut of cats and
dogs)
Incubation period
Months to decades after
exposure
May be years after exposure
1e27 months
Weeks to years after
exposure
1e2 weeks from infection
to onset of pulmonary
symptoms
Pulmonary manifestations
start within 10 days of
exposure, can continue for
more than one month
Several weeks
Investigations Treatment
Hydatid serology positive in Surgery
50-60% Albendazole with or without
Blood eosinophilia praziquantel
uncommon unless cyst Aspiration
leaking
Aspiration and microscopy
Blood eosinophilia Surgical excision
uncommon
Biopsy usually diagnostic
Eggs in stool or sputum Praziquantel
Eosinophilia in peripheral
blood, pleural fluid or
bronchoalveolar lavage
Serology
Serology (may be negative, Tinidazole (or metronidazole)
especially in early disease) followed by diloxanide
Does not cause eosinophilia; furorate or paromomycin
usually does cause
neutrophilia
Larvae in pulmonary, gastric Albendazole, mebendazole,
secretions piperazine, or pyrantel
Eggs in stool in established pamoate
infection with adult worms,
may be absent in larval
migratory phase
Blood eosinophilia during
larval migration
Blood eosinophilia during Albendazole, mebendazole or
migration, which may persist pyrantel pamoate
Eggs in stool in established
infection with adult worms
Eggs may be absent in larval
migratory phase
Peripheral blood eosinophilia Albendazole for visceral
common disease
Eosinophilia in
bronchoalveolar lavage
Toxocara serology
Continued
Review
 Review

therapy), a hyperinfection syndrome can result in severe

Ivermectin, albendazole less

Diethylcarbamazine with or

Thorax: first published as 10.1136/thx.2009.132217 on 29 September 2010. Downloaded from http://thorax.bmj.com/ on May 9, 2021 by guest. Protected by copyright.
disseminated infection which may cause Gram-negative sepsis
and death. Respiratory symptoms may be non-specific and,

without albendazole
apart from gastrointestinal complaints, symptoms of asthma
might be the only feature. In patients with new onset bronchial
Praziquantel
Treatment

asthma or worsening of asthmatic episodes concurrent with

effective
immunosuppression, S stercoralis infection should be considered,
especially in patients from endemic countries.49 50 In immuno-
suppressed patients with hyperinfection, symptoms and signs
consistent with adult respiratory distress syndrome may be

No microfilariae in peripheral
sputum in chronic infection;
Blood eosinophilia common
Larvae in stool or duodenal
sputum, or bronchoalveolar

seen.51 52 In disseminated disease, extensive intra-alveolar

aspirate but not usually in
haematobium) after about

positive after 6-12 weeks

Chronic disease: eggs in

In hyperinfection also in
sputum, body fluids on
Acute disease: eggs in

haemorrhage has been reported and should be considered as

Strongyloides serology
Schistosomal serology

microscopy or culture

Filarial serology (IgG)

eosinophilia common
Acute disease: blood

lavage after 6 weeks

stool and/or urine (S

a cause of acute deterioration.53

Blood eosinophilia
Investigations

Radiological findings
In Strongyloides hyperinfection, pulmonary infiltrates are the most
6 weeks

frequent feature seen on chest radiography. Radiographic changes

blood
may include miliary nodules, reticular opacities and airspace
opacities ranging from multifocal to lobar distribution. These are
thought to be due to secondary infection, haemorrhage, inflam-
infection; hyperinfection may
Acute disease: 5e7 weeks

Pulmonary symptoms may

matory pneumonitis and bacterial abscess formation.13 52 If

occur up to decades after

Up to years after leaving

Chronic disease: years

occur days after acute

widespread air space shadowing is seen on chest radiography,

Incubation period

adult respiratory distress syndrome should be strongly suspected.

after exposure.

Rare manifestations of pulmonary strongyloidiasis include gran-

endemic area

ulomatous changes leading to pulmonary fibrosis.54

infection

Laboratory investigations
Blood eosinophilia is seen in more than 75% of patients with
chronic infection but may be absent in the hyperinfection
syndrome in immunocompromised patients.55 A definitive diag-
Geographical distribution

Asia, sub-Saharan Africa,

nosis is made by demonstration of rhabditiform larvae in stool,

Africa, South America,
south east Asia, China

Worldwide distribution
where sanitation poor

sputum or duodenal aspirates. Filariform larvae may also be seen.

Larvae may be identified on direct microscopy but specialised
South America

culture techniques are more likely to yield positive results.

Antibody assays have sensitivities of approximately 90%;
however, cross-reactions occur with other helminth infections
and antibody levels may be low in immunocompromised
patients.
granulomatous lung disease,

pulmonary infiltrates, miliary

Management
In hyperinfection syndrome:

nodules, airspace opacities

ARDS in severe disease,
pulmonary hypertension,
Acute disease: transient

Treatment with ivermectin is usually effective. In cases of

reticulonodular changes

Bilateral reticulonodular
pulmonary AV fistulae

rarely granulomatous

hyperinfection, repeated treatments are required and expert

Imaging features

lymphadenopathy

parasitological advice should be sought.28 56e58

Chronic disease:

Mediastinal
shadowing

Tropical pulmonary eosinophilia

changes

Presentation
Tropical pulmonary eosinophilia (TPE) typically results from
a hypersensitivity reaction to the lymphatic filarial parasites
Wuchereria bancrofti and Brugia malayi found in endemic regions
asthma, ARDS, intra-alveolar
fever with cough, dyspnoea,

In hyperinfection syndrome:

Fever, malaise, weight loss

Chronic disease: dyspnoea,

Cough, dyspnoea, wheeze

of south east Asia, India, China and Africa. The most common
Acute disease: Katayama

pulmonary hypertension

clinical manifestation of filariasis is elephantiasis resulting from

rash, and arthralgias
Loeffler’s syndrome,

filarial obstruction of lymphatic vessels. The syndrome of TPE is

thought to be an immunological response to microfilariae rather
Presentation

haemorrhage
pneumonitis

than acute infection. Clinically, TPE typically has slow onset

over several months, with respiratory symptoms including
cough, dyspnoea and wheeze which may be worse at night.
Systemic features including fever, malaise and weight loss may
occur. By contrast, Loeffler’s syndrome is caused by larval
migration of nematodes such as Strongyloides, Ascaris or hook-
Table 1 Continued

worm which results in wheeze, cough and dyspnoea of acute

eosinophilia (filariasis)

onset and rarely lasts more than a few weeks.

Tropical pulmonary
Schistosomiasis

Strongyloidiasis

Radiological findings
Bilateral fine nodular or reticulonodular shadowing have been
Condition

described on plain chest radiography.59 However, it has been

suggested that a CT scan of the thorax might be more sensitive

534 Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217


to detect reticulonodular pulmonary opacities and mediastinal
lymphadenopathy.60
Laboratory investigations
High titres of antifilarial antibodies and peripheral blood eosin-
ophilia are present. The extensive immune response leads to
rapid clearance of microfilariae from the blood and, in order to
diagnose TPE, it is essential that no microfilariae can be found in
the peripheral blood. Total serum IgE is raised, as are filarial-
specific IgE and IgG antibody levels. Bronchoalveolar lavage may
show evidence of an eosinophilic alveolitis with a high concentra-
tion of eosinophils.61 Specific antifilarial IgE and IgG antibodies
have also been detected in bronchoalveolar lavage samples.62
Management
Pulmonary abnormalities usually progressively worsen without
treatment. Concomitant infection with other filarial species
must be investigated prior to treatment. Treatment is usually
with diethylcarbamazine under expert guidance; however, it is
sometimes given in combination with albendazole to improve
efficacy.63 64 Even after treatment, pulmonary symptoms may
progress and interstitial lung disease might develop leading to
chronic respiratory failure.65
Non-infectious causes of pulmonary eosinophilia
Other causes of pulmonary eosinophilia need to be considered
in the differential diagnosis of parasitic lung infections. Idio-
pathic lung diseases such as acute eosinophilic pneumonia,
chronic eosinophilic pneumonia and idiopathic hyper-
eosinophilic syndrome and lung diseases of known cause such
as allergic bronchopulmonary aspergillosis, bronchocentric
granulomatosis, drug reactions and eosinophilic vasculitis
(ChurgeStrauss syndrome) can cause pulmonary and peripheral
blood eosinophilia.66 67
CONCLUSIONS
This review outlines the symptoms, signs, investigation and
treatment of parasitic lung diseases which are summarised in
table 1. The clinical presentation and radiology of many of these
diseases may share common features with tuberculosis and
malignancy. When symptoms of lung disease are associated with
gastrointestinal, hepatobiliary or cutaneous symptoms or
a peripheral eosinophilia, there should be a high index of
suspicion for parasitic diseases. With increasing travel and
migration, it is important to consider parasitic infections in the
differential diagnosis of lung diseases. Parasitic lung infections
have been described in patients following chemotherapy or
transplantation and need to be considered in the differential
diagnosis of lung infections in immunocompromised individu-
als.68e70 Direct identification of the causative organisms may be
achieved definitively through microscopic examination of stool
or respiratory tract samples, or indirectly via serological testing.
If identified early, most parasitic lung diseases are curable with
medical treatment. Further information on the distribution of
parasitic lung diseases and treatment may be obtained from the
World Health Organization.28 71
Funding PLC and AG are supported by the UCL Hospitals Comprehensive Biomedical
Research Centre Infection Theme. AG was supported by a Public Health Career
Scientist award from the UK Department of Health.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
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